The etiology of acute gastric mucosal lesions (erosions, ulcerations and diffuse bleeding) is unknown. A large number of agents that produce such lesions have well established vascular actions, e.g. histamine, pitressin, serotonin. In addition ligation of arteries and veins to the rat stomach results in acute mucosal lesions. These findings constitute evidence favoring an important role for vascular alterations in the etiology of this entity. However detailed information concerning the pharmacologic action of the vasoactive agents on the gastric microcirculation and the microcirculatory changes occurring during the induction of mucosal lesions is needed. The use of in vivo microscopy of the gastric microcirculation will permit the determination of a) the specific vascular alterations occurring following the administration of "ulcerogenic" agents (agents that produce acute gastric mucosal lesions), b) whether these changes occur before, during or after the development of mucosal lesions, and c) the comparison of the microcirculation in the region of a developing lesion with that of an uninvolved area of the stomach. The use of the aminopyrine clearance technic or the indicator fractionation technic with Rb86 will permit the determination of the quantitative changes in mucosal blood flow occurring at different time intervals after the administration of the agents, and the temporal relation of these changes to the development of acute mucosal lesions. The objectives of the program is to ascertain by the study of microcirculatory alterations in relation to the development of lesions, whether these changes precede and possibly predispose to mucosal damage. If this does occur, there might be a uniform pattern of vascular alteration that would permit postulation of a vascular theory of etiology, e.g. slowing of mucosal venous drainage results in mucosal plethora, local hypoxia and decreased resistance to acid-peptic digestion.